| Project/Area Number |
18390279
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OGAWA SEISHI The University of Tokyo, HOSPITAL, ASSOCIATED PROFESSOR (60292900)
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| Co-Investigator(Kenkyū-buntansha) |
KUMANO Keiki The University of Tokyo, HOSPITAL, ASSOCIATED PROFESSOR (90396721)
HANGAISHI Akira The University of Tokyo, HOSPITAL, ASSISTANT PROFESSOR (20344450)
ASAI Takashi The University of Tokyo, HOSPITAL, ASSISTANT PROFESSOR (10376436)
鈴木 隆広 東京大学, 医学部附属病院, 助教 (40345210)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥17,400,000 (Direct Cost: ¥15,600,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2007: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2006: ¥9,600,000 (Direct Cost: ¥9,600,000)
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| Keywords | CANCER / GENETICS / ALLELIC IMBALANCES / MICROARRAY / LEUKEMIA |
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| Research Abstract |
The purpose of this project is to explore the genetic basis of hematopoietic malignancies through genome-wide analysis of genetic lesions in a variety of blood cancers, using SNP genotyping microarrays. We performed SNP array analysis of more than 1500 blood cell cancers including acute leukemia usand lymphoma in 2006, and interrogating the target genetic lesions in these cancers based on the SNP array data. A number of candidate lesions have been identified though the analysis. For example, through the analysis of 399 pediatric ALL, we identified novel fusion genes in which PAX5 is a common fusion partner We found that PAX5, an essential transcription factor in B cell development, is fused with a variety of partner genes and that the fusion products inhibit normal functions of PAX5 in a dominant negative fashion. On the other hand, through the analysis of 171 MDS samples, we showed that about 30% of MDS cases have copy number neutral LOB which preferentially involves particular genomic loci. Furthermore, we identified a novel target of MDS, mds11, which are tightly associated with 11qUP'D. It was mutated〜6% of MDS and the mutant mds11 strongly transform 3T3 fibroblase in vitro in a dominant manner We also disclosed other targets or candidates of targets from non-Hodgikin lymphoma and adult T Dell leukemia, which are currently under investigation.
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